Factor v Leiden and antiphospholipid antibodies in either mothers or infants increase the risk for perinatal arterial ischemic stroke.
OBJECTIVE
The objective was to investigate the role of infant and maternal thrombophilia in a cohort of mothers and infants presenting with perinatal arterial ischemic stroke.


METHODS
Forty-seven infants with clinically and radiologically confirmed perinatal arterial ischemic stroke underwent thrombophilia workup: factor V Leiden (FVL), PII20210A mutation, Methylene-tetrahydrofolate reductase 677T polymorphism, protein C, protein S, antithrombin, FVIII, and antiphospholipid antibodies. Thrombophilia data were available for 23 mother-infant pairs and compared with control populations to evaluate the risk for PAS.


RESULTS
Thirty of 47 (64%) infants and 15 of 22 mothers (68%) had evidence of thrombophilia. In 18 of 23 (78%) mother-infant pairs, there was at least 1 thrombophilic risk factor, but 15 pairs were mismatched in pathology. Among infants, FVL, protein C deficiency, and presence of antiphospholipid antibodies prevailed (OR, 4.2; 95% CI, 1.5-11.3; OR, 12.2; 95% CI, 2.5-59.9; OR, 4.1; 95% CI, 1.4-12.2, respectively). Interestingly FVL prevailed in almost one-third of mothers (OR, 8.5; 95% CI, 4.1-17.5) and 18% of mothers had antiphospholipid antibodies (OR, 3.8l; 95% CI, 1.5-10.0).


CONCLUSIONS
Maternal and neonatal thrombophilia, especially presence of FVL or antiphospholipid antibodies, may be important in the pathogenesis of perinatal arterial ischemic stroke. The nature of thrombophilic mother-infant risk potential interactions warrants further investigation.
Simchen
Michal J
MJ
Thrombosis Unit, National Hemophilia Center, Sheba Medical Center, Tel-Hashomer, Israel. gili.kenet@sheba.health.gov.il
Goldstein
Gal
G
Lubetsky
Aaron
A
Strauss
Tzipi
T
Schiff
Eyal
E
Kenet
Gili
G
D000293:Adolescent; D001323:Autoantibodies / Q000032:analysis / Q000097:blood*; D015415:Biomarkers / Q000032:analysis; D002545:Brain Ischemia / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology; D002648:Child; D002675:Child, Preschool; D015331:Cohort Studies; D005165:Factor V / Q000235:genetics*; D005260:Female; D005819:Genetic Markers / Q000235:genetics; D020022:Genetic Predisposition to Disease / Q000235:genetics; D006801:Humans; D007223:Infant; D007231:Infant, Newborn; D008297:Male; D008431:Maternal-Fetal Exchange / Q000235:genetics / Q000276:immunology; D009154:Mutation / Q000235:genetics; D010743:Phospholipids / Q000276:immunology*; D011247:Pregnancy; D011446:Prospective Studies; D012307:Risk Factors; D020521:Stroke / Q000235:genetics* / Q000276:immunology / Q000473:pathology; D019851:Thrombophilia / Q000235:genetics* / Q000276:immunology / Q000473:pathology
D001323:Autoantibodies; D015415:Biomarkers; D005819:Genetic Markers; D010743:Phospholipids; C095381:factor V Leiden; D005165:Factor V